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A craniofacial morphology study of patients with obstructive sleep apnea

By

Dr. OSAMA BAHAA MOHAMMED

Thesis submitted in fulfilment of Requirements for the Degree of Master of Science In Orthodontics

School of Dental Sciences Health Campus

Universiti Sains Malaysia

November 2005

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DEDICATION

To my parents, for their unconditional love, support and encouragement during my work.

To my sisters, Aseel, Hadeel whose love and support made this possible.

To my in-law, Bashar, Raed, and my sweet nieces, Basma and Salim. Your smiles are all I need for encouragement.

THANK YOU

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TABLE OF CONTENTS

Page

DEDICATION ……… iii

ACKNOWLEDGEMENTS ……… iv

TABLE OF CONTENTS ……… vi

LIST OF TABLES ……… xii

LIST OF FIGURES ……… xiii

LIST OF ABREVATION GLOSSARY ……… ……… xv xvii ABSTRACT ……… xviii

ABSTRAK ……… xx

CHAPTER ONE INTRODUCTION 1.1 Background ……… 1

1.2 Statement of the problem ………. 4

CHAPTER TWO LITERATURE REVIEW 2.1 Introduction ……… 5

2.2 Sleep apnea ……….…. 7

2.3 Classification of Sleep Apnea ………. 8

2.3.1 Obstructive Sleep Apnea Syndrome ………. 8

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2.3.2 Central Sleep Apnea ……… 10

2.3.3 Mixed Sleep Apnea ……….. 12

2.4 Hypopnea ………..………… 13

2.5 Apnea, hypopnea, and apnea + hypopnea indices 14

2.6 Upper airway resistance syndrome ……… 14

2.7 Upper airway anatomy……… 16

2.8 Normal physiology of upper airway ……….. 18

2.9 Pathophysiology of the upper airway ……….……….. 20

2.9.1 Shape and position of the tongue ……… 22

2.9.2 Shape and position of the soft palate……… 25

2.9.3 Morphology of the uvula ………. 26

2.9.4 Role of the tonsils and adenoids ……….. 27

2.9.5 Nasal congestion ………. 29

2.9.6 The influence of craniofacial structure... 32

2.9.7 The hyoid bone position ... 35

2.10 Occurrence of obstructive sleep apnea ………. 36

2.10.1 Prevalence ……… 36

2.10.1.1 Sex ……… 37

2.10.1.2 Age ……… 39

2.10.1.3 Ethnicity ……… 40

2.11 Risk factors with particular population health significance 41 2.11.1 Obesity ……… 41

2.11.2 Alcohol ……… 44

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2.11.3 Smoking ……… 45

2.11.4 Hormonal influences ……… 46

2.12 The Cost of obstructive sleep apnea in the population 48 2.12.1 Hypertension ……… 48

2.12.2 Cardiovascular morbidity and mortality ………. 49

2.12.3 Sleepiness ………. 50

2.12.4 Motor vehicle crashes and occupational accidents 52

2.13 Justification of the study ……….. 53

CHAPTER THREE OBJECTIVES AND HYOTHESIS 3.1 General objective ……… 54

3.2 Specific objective ... 54

3.3 Hypothesis ……… 54

CHAPTER FOUR MATERIALS AND METHODS 4.1 Study design ………. 55

4.2 Population and sample ………... 55

4.2.1 Source of population ……… 55

4.2.2 Sampling frame ………. 57

4.2.2.1 Inclusion criteria ……… 57

4.2.2.2 Exclusion criteria ………. 58

4.2.3 Sampling size (objectives one, two, three) ………….. 58

4.2.4 Data collection procedure ………... 58

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4.3 Research Tools ……… 60

4.3.1 Polysomnography (PSG) ………... 60

4.3.2 Physical examination ………... 65

4.3.2.1 Neck circumference (NC) ………... 65

4.3.2.2 Body mass index (BMI) ………... 65

4.3.2.3 Size of tonsils ……….. 67

4.3.3 Dental study model ……….. 68

4.3.4 Lateral cephalometric radiograph ……… 71

4.3.5 Posterior-anterior cephalogram ………. 79

4.3.6 Computed tomography (CT scan) ………. 81

4.3.7 Computerized X- ray systems ……… 87

4.4 Reproducibility of the measurements ……… 88

4.5 Analysis of data ……… 92

4.6 Ethical approval ……… 92

CHAPTER FIVE RESULTS 5.1 Profile of the study ...……… 93 5.2 Differences of the maxillary dental cast morphometric study

in OSA and control groups

95

5.3 Differences of the mandibular dental cast morphometric study in OSA and control groups

96

5.4 Differences of the measurements in Lateral cephalometric X-ray in OSA and control groups

97

5.5 Differences of the measurements in posterior-anterior X-ray in OSA and control groups

101

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5.6 The CT scan finding in OSA patients ……… 102

CHAPETR SIX DISCUSSION

6.1 General discussion ………. 107

6.2 The role of obesity in OSA patients ……… 109

6.3 Maxillary and mandibular dental cast morphometric …. 110

6.4 Cephalometric findings ……… 111

6.4.1 The length and width of the soft palate ……… 111 6.4.2 The length and width of the tongue ………. 112 6.4.3 The upper, middle and lower posterior airway spaces 113

6.4.4 The hyoid bone position ……… 115

6.4.5 The maxillary and mandibular discrepancy ……… 116 6.4.6 The lower face height, posterior face height and to total face

height

117

6.4.7 The cranial base length and cranial base flexure angle 118 6.5 The posterior anterior X-ray assessment ……… 119

6.6 The CT scan findings ……….. 120

CHAPTER SEVEN CONCLUSION AND RECOMMENDATION n

7.1 CONCLUSION ………. 122

7.2 Recommendation for future research ……… 123

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References ……… 124

Appendices ……… 134

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ACKNOWLEDGEMENTS

First of all. I would to thank God for giving me the strength and courage throughout the duration of this research project.

There are times when words are inadequate. I grant my grateful appreciation and thanks to all those who have contributed to this work.

I wish to express my greatest appreciation and gratitude to my supervisor Prof. Dr. Ab.

Rani Samsudin, for his persistent motivation, support, farsighted guidance and leadership throughout my research project.

My sincere and special gratitude to my co-supervisor Dr. Rozita Hassan, for her guideness, great knowledge of clinical work, continual support and advice throughout my study.

My respect and appreciation to Dr. Akbar, and Dr. Norehan the specialists of orthodontic department for contribution and support in the clinic.

I would like to extend my thanks Dr. Karima for her time, efforts, help and contribution to my research.

Dr. Mohd Ayub for his expert analytical and mathematical contributions to this project.

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My special thankful and appreciation to Dr. Karim Alwan for his continual support, great help, and advice.

Special thanks to En. Hakim, Firdaous, Aida, and Aida the research officers in the dental school, USM, for their kind assistance and providing facilities for sample collection.

I’m also thankful to sleep laboratory technologist Suhailah and Yusman for their invaluable help in sample collection.

Finally, I owe a lifetime and my deepest gratitude to my father Prof. Dr. Bahaa Mohammed, who support, and guideness throughout my research.

To all named and unnamed helpers and friends, I again extend my thanks.

Dr.OSAMA BAHAA MOHAMMED

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LIST OF FIGURES

Figure Page

Figure 2.1 Graph showing the attempt of the respiratory muscles to breath 9 Figure 2.2 Graph showing no attempt of respiratory muscles to breath 10 Figure 2.3 Diagram showing nasopharynx, oropharynx and hypopharynx 18

Figure 2.4 Abnormal airway during sleep 23

Figure 2.5 Macroglossia 25

Figure 2.6 Elongated uvula 27

Figure 2.7 Hypertrophy of tonsil 29

Figure 2.8 Retrognathia 32

Figure 2.9 Patient with Pierre Robin syndrome 33

Figure 2.10 Patients with Apert’s Syndrome 35

Figure 2.11. An obese young boy with short, thick neck typically seen in patients with obstructive sleep apnea

42

Figure 4.1. The sleep study station to observe the patient during the sleep study

56

Figure 4.2. The sleep science laboratory suit where the patient sleep during polysomnography

56

Figure 4.3 Flow chart of the study 59

Figure 4.4 Diagram showing the places of PSG putting on the body of the patient

60

Figure 4.5 The patient being hocked to PSG machine 62

Figure 4.6 Measurement of neck circumference 66

Figure 4.7 Measurement Body mass index 67

Figure 4.8 Digital caliper to measure study model 68

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Figure 4.9 Maxillary dental cast measurements 69

Figure 4.10 Mandibular dental cast measurements 70

Figure 4.11 Soft tissue reference lines on lateral cephalometric 75 Figure 4.12 Skeletal reference lines and angles on lateral cephalometric 76 Figure 4.13 The lines measure the division of the anterior and posterior

cranial base

77

Figure 4.14 Nasion-sella-basion angle which represents the measurement of the cranial base flexure

78

Figure 4.15 The posterior-anterior landmarks 80

Figure 4.16 Flow chart of the CT scan procedure 82

Figure 4.17 Sagittal view show the CT scan Levels 83

Figure 4.18 Axial view show the nasopharyngeal level . 84 Figure 4.19 Axial view show the oropharyngeal level . 85 Figure 4.20 Axial view show the hypopharyngeal level . 86 Figure 4.21 The researcher during using computerized X- Ray Systems 87 Figure 5.1 The distribution of male to female in OSA group 94 Figure 5.2 The nasopharyngeal level showing a significant narrowing in

anterior posterior (length) dimension and medial lateral (width) dimension

104

Figure 5.3 The oropharyngeal level showing a significant narrowing in anterior posterior (length) dimension and medial lateral (width) dimension

105

Figure 5.4 The hypopharyngeal level showing a significant narrowing in anterior posterior (length) dimension and medial lateral (width) dimension

106

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LIST OF TABLES

Table Page

Table 4.1 Showing the function of each parameter in PSG 61 Table 4.2 Reproducibility of measurements of maxillary Dental Cast 89 Table 4.3 Reproducibility of measurements of mandibular Dental Cast 89 Table 4.4 Reproducibility of measurements of Lateral Cephalometric x-

ray

90

Table 4.5 Reproducibility of measurements of posterior-anterior x-ray 91 Table 4.6 Reproducibility of measurements of CT scan 91 Table 5:1 Differences of (BMI, and NC) analysis between OSA and

control groups

94

Table 5:2 Differences of the Maxillary Cast Morphometric analysis between OSA and control groups

95

Table 5:3 Differences of the Mandibular Cast Morphometric analysis between OSA and control groups

96

Table 5.4 Differences of Soft palate, Pharyngeal airway space, and Hyoid bone position between OSA and control groups

99

Table 5.5 Differences of Maxillary, Mandibular positions, facial height, and cranial base between OSA and control groups

100

Table 5.6 Differences of the Measurements of Mandibular width, Maxillary width, and Facial width between OSA and control groups

101

Table 5.7 Differences of the Measurements of CT scan between OSA and control groups: (Nasopharyngeal level, Oropharyngeal level and Hypopharyngeal level)

103

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Kajian Morfologi Kranofasial Pesakit- Pesakit Henti Dalam Tidur (Bermasalah Tidur Obstruktif Apnea)

ABSTRAK

Masalah tidur obstruktif apnea (OSA) didefinisikan sebagai pemberhentian pernafasan berulang (apneas) yang berlaku sekurang-kurangnya selama sepuluh saat atau lebih pada sesuatu ketika semasa tidur. Otot pernafasan berusaha merangsang tetapi sekatan di bahagian atas saluran pernafasan menghalang udara dari sampai ke paru-paru. Ini akan menyebabkan penutupan separa atau penuh pada saluran pernafasan bahagian atas yang menyebabkan kesan mudarat keatas kualiti tidur dan pertukaran gas. Keaadaan ini memberi kesan kepada 4% lelaki dan 2% wanita pada peringkat umur pertengahan. OSA adalah satu keadaan yang membahayakan nyawa dimana pesakit mengalami pemberhentian pernafasan berkala ketika tidur. Tujuan kajian ini ialah untuk mengembangkan informasi pengkalan data morfologi kraniofasial tentang morfologi saluran pernafasan bahagian atas dan corak skeletal dalam pesakit OSA dengan membandingkan penemuan yang didapati dengan keputusan dari subjek yang normal dalam kumpulan kawalan. Oleh itu, dua puluh lima orang subjek diambil sebagai pesakit OSA dan dua puluh lima orang sebagai kumpulan kawalan yang dipilih dari Makmal beradu menggunakan polysomnografi.

Semua subjek untuk kajian ini adalah orang dewasa berumur 18 tahun keatas.

Metodologinya termasuklah mengira index jisim badan (BMI), lilitan leher setiap subjek, x-ray cefalometrik lateral, x-ray posterior –anterior, dan model kajian gigi bahagian atas dan bawah juga diambil. Diameter farinks ditentukan dengan mengukur kawasan saluran pernafasan yang paling minimal termasuk panjang dan lebar saluran pernafasan pada bahagian nasofarink, orofarink dan hypofarink, kemudian dibandingkan dengan subjek yang normal menggunakan imbasan CT . Imbasan CT hanya diambil untuk OSA yang

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teruk. Usaha juga dilakukan untuk menentukan kekerapan pesakit untuk tidur dalam situasi yang berbeza menggunakan kajiselidik skala tidur Epsworth. Keputusan menunjukkan terdapat perbezaan signifikan BMI antara pesakit OSA dan kumpulan kawalan (nilai P = .001). BMI meningkat secara signifikan bagi pesakit OSA , lilitan leher pesakit OSA juga meningkat. Panjang lelangit lembut, lebar lelangit lembut, lebar lidah , ruang atas posterior saluran udara, ruang tengah posterior saluran udara, ruang bawah posterior, saluran udara, jarak antara tulang hioid ke plana madibular, jarak dari tulang hioid ke spina hidung, lebar maksilari, dan sudut fleksur tapak kranial berbeza secara signifikan bagi pesakit OSA dibandingkan dengan kumpulan kawalan. Tiada perbezaan yang signifikan antara dua kumpulan kajian dalam inter-kanin, inter-first dan premolar kedua, jarak inter – molar bahagian lengkungan atas dan bawah, protusi maksilari, pronatisma mandibular, ketinggian muka bawah, ketinggian keseluruhan muka, ketinggian muka posterior, lebar muka, lebar mandibular, tapak kranial anterior, dan tapak kranial posterior. Skala tidur Epsworth mempunyai perbezaan yang signifikan bagi pesakit OSA dan grade skala meningkat bagi pesakit OSA. Imbasan CT menunjukkan bahawa pesakit OSA peringkat teruk mempunyai farink yang sempit pada tahap nasofarink, orofarink dan hypofarink.

Kesimpulannya, kelainan ukuran kraniofasial telah dikenal pasti dalam pesakit yang mengalami OSA, dan beberapa kajian dan pengukuran lain perlu untuk mengenal pasti kelainan yang berkaitan dan seterusnya menentukan kaedah yang paling sesuai untuk menguruskannya.

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A CRANIOFACIAL MORPHOLOGY STUDY OF PATIENTS WITH OBSTRUCTIVE SLEEP APNEA

ABSTRACT

Obstructive sleep apnea (OSA) is defined as a repetitive cessations of breathing (apneas) lasting for at least 10 seconds or more for each event during sleep. The respiratory muscles attempt to inspire, but blockages in the upper airway prevent air from reaching the lungs.

This will cause partial (hypopnea) or complete (apnea) closure of the upper airways with consequent adverse effects on sleep quality and gas exchange. The condition affects approximately 4% of men and 2% of women in their middle-ages. OSA is a potentially life- threatening condition in which a patient suffers periodic cessations of breathing during sleep. The aim of this study is to develop a data base on the craniofacial morphology of the upper airway morphology and skeletal patterns in patients with OSA and compare the findings with those of normal subjects in the control group. Twenty-five subjects as OSA patients and twenty-five as the control group were selected from the Sleep Laboratory by using Polysomnography. All the subjects of this study were adults age ranging 18-65 years.

Methodologies include the measurements of the body mass index (BMI), neck circumference, lateral cephalometric X-ray, posterior-anterior X-ray, and upper and lower dental study models were taken. For severe OSA cases, the diameter of the pharynx was estimated by measuring the length and width of the pharynx at the level of nasopharynx, oropharynx, and hypopharynx, and compared with normal subjects by using CT scan. The results showed that there was a significant difference in BMI between OSA patients and control group (P value=.001), the BMI significantly increased in OSA patients, the neck circumference was also increased in OSA patients. The length of soft palate, width of soft

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palate, width of tongue, upper posterior airway space, middle posterior airway space, lower posterior airway space, distance from hyoid bone to mandibular plane, distance from hyoid bone to posterior nasal spine, maxillary width, and cranial base flexure angle were statically significantly different in OSA patients compared to the control group. There were no significant differences between the two study groups in the inter-canine, inter-first and second premolar, inter-molar distances of upper and lower arches, maxillary protrusion, mandibular prognathism, lower face height, total face height, posterior facial height, facial width, mandibular width, anterior cranial base, and posterior cranial base. The CT scan shown that severe OSA patients have narrowing of pharynx at the level of nasopharynx, oropharynx, and hypopharynx. In conclusion, craniofacial morphological differences have been found in patients suffering from OSA as compared to control, and that a number of investigations and measurements are required to detect underlying deformities, to decide for the most suitable management methods.

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CHAPTER ONE INTRODUCTION 1.1 Background

Over the past two decades, medicine and dentistry have increasingly focused on breathing disorders during sleep. The characteristics of obstructive apnea have been described in the medical and classical literatures for decades, in the 19th century Broadbent, who described the perfect silence during sleep through two, three, or four respiratory periods in which accompanied by ineffectual chest movements. Finally air enters with a loud snort, after which there are several compensatory deep inspiration (Jureyda and Shucard, 2004).

The understanding of sleep-disordered breathing has been evolved over the years. The first description of abnormal breathing with polygraphic demonstrations during sleep was first reported in France in 1955, in-patient with Pickwickian syndrome. Pickwickians patients had combination of obesity, edema, cardiac symptoms, and agitated sleep presented abnormal breathing patterns during sleep (Gilleminault and Quo, 2001).

Sleep apnea owes its name to Greek word apnea, meaning “want to breathe” (Yantis, 1999). Sleep apnea is a sleep disordered breathing characterized by repetitive cessation of breathing (apneas) lasting for at least 10 seconds, and occurring 30 times or more during 7 hours of nocturnal sleep (DePonte et al., 1999).

Partial obstructive of the upper airway, termed hypopneas, also affects oxygen saturation, which led to sleep disturbances. These partial obstructions are defined as

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polygraphic events with a reduction of airflow, as measured by thermistor, also lasting more than two breaths.

Investigations using specific polygraphic recordings of normal-weight patients with abnormal breathing during sleep led to the description of the (obstructive sleep apnea) OSA. The definition of the apnea syndrome came from studies that coxexist with excessive daytime sleepiness or related problems in daytime functions (Guilleminault and Quo, 2001).

The discovery of sleep apnea and its various forms and the subsequent elucidation of sleep disorder breathing (SDB) as a major mechanism of sleep pathology became a major impetus for the development of modern sleep medicine. The discovery obstructive sleep apnea (OSA) stimulated vigorous investigations in a new field of respiratory physiology focused on the control of upper airway function awake and in sleep (Nowara, 2001).

Sleep apnea is generally classified into obstructive sleep apnea (OSA), central sleep apnea (CSA) and mixed sleep apnea (MSA). OSA was recognized as the most common disorder with significant morbidity and potential mortality occurring in 2-4% of middle- aged adults. It was characterized by recurrent episodes of partial or complete upper airway obstruction during sleep. These manifest as a decrease in airflow despite ongoing inspiratory efforts. The lack of adequate alveolar ventilation results in oxygen desaturation of at least 3%. Sleep-related obstructive breathing events are characterized by transient (10 seconds or longer) reduction in (hypopnea) or complete cessation of (apnea) respiratory flow. OSA is associated to snoring, obesity, systemic or pulmonary hypertension sleep

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related cardiac dysrhythmias, nocturnal angina, gastroesophageal reflex, impaired quality of life, and insomnia.

CSA, it is less common which caused by some problems in the central nervous system and occur when the brain fail to send appropriate signals to the breathing muscle to initiate breathing causing cessation of all respiratory effort during sleep (Walter and Eliot, 2002).

MSA is the combination of both OSA and CSA. An episode of MSA usually starts with a central component and then becomes finally obstructive in nature (Jonas 2001).

Apnea refers to cessation of nasal and oral airflow. Hypopnea refers to a reduction in airflow to <50% of baseline in association with oxyhaemoglobin desaturation. Apnea – Hypopnea index (AHI) indicating the number of respiratory irregularities per sleep hour.

AHI is calculated as (total number of apneas + hypopnoea) / (Total sleep time in minutes) x60 Obstructive sleep apnea may be mild (AHI < 15 events per hour), moderate (AHI = 15- 30 events per hour), and sever (AHI = >30 events per hour).

1.2 Statement of the problem

OSA is a potentially life-threatening condition in the patient, who suffers periodic cessation of breathing during sleep, which impairs the quality of life (Ang et al., 2004).

Sleep apnea patients appear to have at least twice as much hypertension, ischemic heart disease and cerebrovascular disease. The most serious potential consequence of sleepiness

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is impaired preferences at the wheel while driving and there is convincing evidence that sleepiness is substantial risk factor for driving accidents (McNicholas et al., 2002).

The National Traffic Safety Administration (NHTSA) estimated that the annual cost of motor vehicle accidents related to sleep deprivation totaled $12.4 billion. Other studies have shown that patients with sleep-disordered breathing who had been diagnosed with sleep apnea can have a seven- to 15-fold increase in accident frequency and an eightfold increase in the fault frequency (Bailey and Attanasio, 2001).

It is reported that 40 to 30 million Americans have some type of chronic sleep disturbance, and 20 to 30 million have intermittent sleep–related problem. A survey by the Gallup organization indicated that as many as 65 million Americans have sleep disorders and that 32% of the 65 million reported excessive daytime sleepiness that can interfere with their normal daytime routine (Bailey and Attanasio, 2001).

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CHAPTER TWO LITERATURE REVIEW

2.1 Introduction

Obstructive sleep apnea (OSA) is the periodic reduction (hypopnea) or cessation (apnea) of breathing due to narrowing of the upper airways during sleep. The main symptom is daytime sleepiness, which may lead to premature death, hypertension, ischemic heart disease, stroke, and road traffic accidents. The high prevalence of the syndrome and the morbidity and mortality thought to be associated with it have led to the view that sleep apnea may be as big a public health hazard as smoking (Wright et al., 1997).

The interaction between anatomy and muscle function of the upper airway is considerable importance to understanding the OSA (Ono et al., 1996). The pathophysiologic etiology of OSA includes factors related to the upper airway, especially at the level of the soft palate and the base of the tongue. Other etiologies include, relative mandibular retrognathia, low position of the hyoid bone, decrease in posterior airway space, increased tongue volume, and enlargement of the palatine or adenoidal tissue (Gavish et al., 2000).

Sleep arousal is an important defense mechanism, which was induced by internal stimuli activation of the autonomic nervous system, also called subcortical arousals, which are reflected by abrupt cardiac changes such as heart rate, arterial blood pressure, respiratory change, muscular or galvanic skin responses. The mechanoreceptor-triggered arousal

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depends on the level of negative pressure during aggravated inspiration (Scholle and Zwacka, 2001).

The severity of sleep apnea is defined on the basis of the apnea – hypopnea index (AHI). OSA is defined by the presence of at least 5 obstructive apneas or hypopneas, or both happened per hour while the patient is a sleep. OSA is commonly divided into 3 levels of severity: mild AHI < 15 events per hour, moderate AHI are about 15-30 events per hour, and sever AHI >30 events per hour.

Recently, a survey of health care utilization among OSA patients showed that during the 10 years before diagnosis they had already been heavy users of health services for several years. The estimated cost of this care was twice as much as that of average patients.

This finding reflected the underlying risk factors such as obesity, alcohol and tobacco consumption in OSA patients (Tangugsorn et al., 2001).

The prevalence of OSA was 4% in men and 2% in women 30 to 60 years of age, and it may be much higher among elderly persons. A recent publication from The National Center on Sleep Disorders Research at the National Heart, Lung, and Blood Institute suggested that sleep apnea is common as asthma (Millman, 1999).

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7 2.2 Sleep Apnea

Sleep apnea is defined as a repetitive cessation of breathing (apneas) lasting for at least 10 seconds, and occurring 30 times or more during 7 hours of nocturnal sleep (Francesco, 1999).

Sleep apnea is a potentially life-threatening condition in which the patient suffers periodic cessations of breathing during sleep, which impairs the quality of life. The main presentation is loud snoring which the individual is usually not aware, the irregular breathing patterns and restless movements in bed characterize of this disorder.

The sleep apnea syndrome represents something of a paradox in clinical medicine. On the one hand, this disorder has been recognized only in recent decades, and it is still regarded as a niche interest by many clinicians, particularly those from clinical disciplines other than respiratory medicine, neurology and otolaryngology. On the other hand, the syndrome is now recognized as being very common and current epidemiological data indicate that sleep apnea syndrome is second only to asthma in the prevalence league table of chronic respiratory disorders. Further more, there is increasing evidence that the sleep apnea syndrome is associated with a considerable number of adverse sequel in both behavioral and physical condition. Behavioral consequences include daytime sleepiness, impaired concentration and neuropsychological dysfunction, where as physical consequences include cardiovascular disorders, particularly hypertension (McNicholas et al., 2002).

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8 2.3. Classification of Sleep Apnea

2.3.1 Obstructive Sleep Apnea

Obstructive sleep apnea (OSA) is characterized by repetitive upper airway obstruction and increased upper airway resistance, leading to high negative intrathoracic pressure with consequent increased work of breathing, alveolar hypoventilation with hypoxemia, abnormal autonomic function, frequent arousal, movement of the legs or body, sleep fragmentation and derangement of sleep architecture (Lin et al., 2003).

OSA is a common disorder affecting approximately 4% of men and 2% of women in the middle-aged workforce. Snoring is a precursor to OSA, which is more common affecting 40-60% of adults. These disorders result from sleep-related narrowing of the upper airway, which is though to be to varying combinations of anatomical and neuromuscular factors that culminate in an imbalance of forces acting on the airway. The respiratory muscles attempt to inspire, but a blockage in the upper airway prevents air from reaching to the lung (Figure 2.1). The figure show stop of nasal flow while the muscles of thorax and abdomen continue attempt to breath, also it show decrease in oxygen saturation.

This will causes partial (hypopnea) or complete (apnea) closure of the upper airway, with consequent adverse effects on sleep quality and gas exchange.

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OSA is an important widely prevalent public health problem. The typical symptoms during sleep are apnea, snoring, dyspnea, and choking episodes. Once apnea or hypopnea develops, recurrent arousal causes excessive sleepiness and cognitive decreases during the daytime. The combination of acute and chronic haemondynamic effects in obstructive sleep apnea have been associated with increased risk of myocardial infarction, cerebrovascular accidents, hypertension, and congestive heart failure.

Figure 2.1 Graph showing the attempt of the respiratory muscles to breath (Adapted from sleep science laboratory, Hospital Universiti Sains Malaysia)

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10 2.3.2 Central Sleep Apnea (CSA)

Central apnea is defined as 10 seconds or more of no airflow without ventilatory effort (Figure 2.2). The figure show stop of nasal flow and the muscles of the thorax and abdomen also do not attempt to breath. Central sleep apnea (CSA) is diagnosed if the frequency of central apneas and hypopneas exceed 5 per hour and is accompanied by symptoms of daytime sleepiness. CSA is thought to develop when a stimulus by hypoxemia, arousals, and pulmonary congestion results in periods of increased ventilation and subsequent decline in CO2 (Hahn and Staats, 2004).

CSA constitutes a heterogeneous group of disorders whose common feature is a momentary cessation of breathing during sleep due to a transient withdrawal of central

Figure 2.2 Graph showing no attempt of respiratory muscles to breath(Adapted from sleep science laboratory, Hospital Universiti Sains Malaysia)

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respiratory drive to the muscles of respiration. Thus, in contrast to OSAS, in which respiratory drive continues during apnea, in CSA no respiratory efforts or intrathoracic pressure swings are generated.

The clinical evaluation and treatment of these disorders is challenging because they are relatively uncommon, which can arise from entirely different underlying causes, and have widely varying clinical presentations. Increases in CO2 generally result from reductions in ventilation or outright apneas due to an underlying depression of respiratory drive (Walter and Eliot, 2002).

The CSA patient’s having a loss of oxygen to the lung caused by the respiratory chest muscles make no attempt to breath as a result of central nervous system disorder. In patients with idiopathic central hypoventilation, pulmonary function test results typically are normal, unless there is coexisting lung disease, and tests of respiratory strength also are normal. The apnea and hypopnea that occur in association with central hypoventilation syndrome, the central feature of sleep hypoventilation is an abnormal increase in CO2

during sleep (Walter and Eliot, 2002).

Since no airway obstruction is present in CSA, it seems that central and peripheral chemoreceptors play a more prominent role. It is generally accepted that the rapidly responding peripheral chemoreceptors are the most likely cause of feed-related respiratory instability (Verbraecken et al., 1998).

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12 2.3.3 Mixed sleep apnea (MSA)

MSA is due to an absent ventilatory effort (a ‘central’ pattern), and subsequently persists despite resumption of ventilatory efforts (an ‘obstructive’ pattern).

Central apneas can predispose to obstructive apneas. During central apnea, the central drive to the respiratory muscles is withdrawn and airflow ceases, thus the anatomically predisposed pharyngeal airway becomes compliant and is susceptible to collapse during the subsequent inspiration (Hahn and Staats, 2004).

Patients with OSA who also have prolonged central apnea should undergo imaging studies of the brainstem, most accurately performed by magnetic resonance imaging.

Particular attention should be directed to the brainstem and cervico-medullary junction for evidence of a Chiari malformation or space-occupying lesion (Kirk et al., 1998).

Mixed apneas contain polysomnographic characteristics consistent with a central and obstructive component. There is evidence, however, that the central compound of a mixed apnea is actually a prolongation of exhalation against an obstructed upper airway or a brief expiratory apnea before the resumption of cyclic respiratory efforts.

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13 2.4 Hypopnea

Hypopnea is defined as an event which is characterized by disproportionate reduction of inspiratory airflow relative to inspiratory effort or metabolic needs. The American Academy of Sleep Medicine Task Force defined or characterized hypopnea as follows:’ A clear decrease (>50%) from baseline in the amplitude of a valid measure of breathing during sleep or an amplitude reduction (<50%) associated with either an oxyhemoglobin desaturation (>3%) or an arousal, and the event should last at least 10 seconds. Hypopneas, like apneas, can be central or obstructive, although this distinction is infrequently made when reporting clinical sleep studies (Jonas et al., 2001).

Gould et al. (1987) have observed a number of patients with full clinical picture of the obstructive sleep apnea syndrome who have had no apnea at all but instead have had recurrent episodes of nocturnal hypoventilation. In the absence of apneas, these patients cannot be said to have the sleep apnea syndrome, which was originally defined purely in terms of nocturnal apnea frequency. Further confusion is caused by disagreement as to the definition of a hypopnoea, some describing them as a decrease in the airflow signal, some as a decrease in thoracoabdominal movement, and others as a decrease in the airflow in association with 4% drop in oxygen saturation.

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2.5 Apnea, Hypopnea, and Apnea + Hypopnea Indices

Dividing the total number of apneas during a recording period by the total sleep time yields the average number of apneas per hour of sleep, or apnea index (AI). Similarly a variety of other indices, including hypopnea index (HI) and apnea + hypopnea index (AHI) (also termed the respiratory disturbance index RDI)) are usually employed to quantify OSAS severity. The concept of ‘index’ permits standardization of event frequency for the number of hours slept. This facilitates the comparison of individual patient data with normative as well as pre- and post – treatment values (Jonas et al., 2001).

Alternatively, the AHI can be considered similar to blood pressure, with increasing values indicative of increasing disease severity. The advantages of using the AHI to classify disease status include its relative simplicity and high night-to-night reproducibility.

The disadvantages of using AHI as a sole indicator of disease include the between- laboratory variability in measurement technique, its lack of informativeness regarding the severity of individual events (duration, associated hypoxemia and arousal) and its uninformativeness regarding the functional and physiological impact of the disorder (Redline and Tishler, 2000).

2.6 Upper Airway Resistance Syndrome

The upper airway resistance syndrome (UARS) is defined by repetitive and progressively increasing inspiratory efforts with subsequent transient arousals, but without associated reduction in airflow (Jonas et al., 2001). Bader (2000), described the combination of habitual heavy snoring, increased upper-airway resistance, sleep

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fragmentation, and daytime sleepiness is referred to as the upper-airway resistance syndrome.

Patients with UARS will go to sleep, then begin loud, crescendo snoring which leads to an arousal or awakening. This arousal is followed by the patient’s falling back to sleep, resumption of snoring, and awakening again. These patients may exhibit all the clinical symptoms of OSA but without apneic or hypopneic events. Upper airway resistance syndrome is not a well-defined condition, and its diagnosis is therefore difficult. These patients are presently treated if they had OSA.

Patients with OSAS and UARS complain of day time tiredness, fatigue, and variable degrees of sleepiness. There was no difference in daytime sleepiness and daytime tiredness between the OSAS and UARS. Several hypotheses may be proposed to explain the differences in sleep electroencephalogram activity seen in OSAS and UARS patients. The differences suggest that both groups of patients have different cortical responses to abnormal respiratory challenges during sleep. There may be a different integration of messages from the periphery (i.e. respiratory apparatus) in the central nervous system (Gilleminault et al., 2001). There are indications that the microstructure of nocturnal sleep is different in UARS and OSAS, and patients with OSAS present more important drops in oxygen saturation with their abnormal breathing events than UARS patients. But further research is needed to understand the exact relationship between the two clinical entities (Gilleminault et al., 2000).

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During nasal breathing the nasal passages constitute a relevant upstream inspiratory resistor whereas during mouth breathing the oral cavity is the potential site of upstream resistance. The resistance to airflow through the oral cavity is a major component of total upper airway resistance during oral and oronasal breathing. Mouth breathing occurs during sleep, even in normal subjects, and may be increased during sleep disordered breathing events (Lin et al., 2003).

2.7 Upper Airway Anatomy

The anatomy of the upper airway, including the oral cavity, begins with intake of air through either the nose or the mouth. The critical component controlling the airway function are the muscles that control airway dimension or opening and are related to the primary structures of the airway, such as the tongue, soft palate, and uvula as well as the upper and lower pharynx. Some hard structures need to be considered, especially within the nose (Bailey, 2001).

The upper airway is generally divided into three regions based on midsagittal anatomy.

These regions are first, the nasopharynx (the nasal turbinates to the hard palate). Second, the oropharynx, which is subdivided into a. retropalatal (the level of the hard palate to the caudal margin of the soft palate) and b. the retroglossal (the caudal margin of the soft palate to the base of the epiglottis) regions; and third, the hypopharynx, (the base of the tongue to the larynx) (Figure 2.3) (Schwab, 2001).

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Upper airway dilator muscles play an important role in the determining the upper airway collapsibility. The dilating force developed by these muscles is only one that counterbalances the collapsing forces represented by the negative transmurul pharyngeal pressure and by the weight of upper airway structures.

At the pharyngeal level there is no bony or cartilaginous structure on maintain the aperture of the upper airway. Therefore, the maintenance of upper airway patency depends on the force developed by the contraction of upper airway dilators (Series, 2002). The pharynx extends superoinferiorly from the base of the cranium to the level of the inferior surface of the body of the 6th cervical vertebra. The pharynx lies dorsal to the nasal cavity, the oral cavity, and the larynx.

The contraction of the diaphragm against the high resistance offered by the nose during inspiration creates a subatmospheric intra-airway pressure which may narrow the collapsible pharyngeal segments in the pharynx. There are three collapsible pharyngeal segment which include the retropalatal pharynx as a velo- or nasopharynx, posterior to the soft palate, the retroglossal pharynx where oropharynx, posterior to the tongue from the tip of the uvula to the tip of the epiglottis) and the retroepiglottic pharynx (laryngo- or hypopharynx, posterior to the epiglottis). These pharyngeal segments are collapsible because the anterior and lateral walls lack bony support. The adult human is the only mammal to have an oropharynx (in all other mammals the tip of the uvula touches the tip of the epiglottis) and to suffer from OSA (Benumof, 2001).

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18 2.8 Normal Physiology of Upper Airway

The upper airway is basically a soft tissue tube, the patency of which is maintained in part by the activity of muscular groups of which the tensor veli and genioglossus muscles are highly important members. The action of these muscle groups has an important influence on the physiology of sleep disorders.

The upper airway is a complex structure with many competing physiological functions, including swallowing, speech and breathing. It is richly innervated and its mechanical behavior is influenced by a multitude of neural controls and reflexes (Ayappa and Rapoport, 2002).

Figure 2.3 Diagram showing nasopharynx, oropharynx and hypopharynx (Adapted from www.dentalresource.com)

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According to the “balance of the pressures” concept, the size and the resistance of the airway depends on the balance between collapsing intraluminal pressures generated during inspiration by subatmospheric pressures in the thorax and outward contraction forces of the upper airway dilator muscles. Patency of the airway depends on transmurul pressure (Ptm), which is the different between the negative intraluminal pressure caused by inspiratory efforts and the positive pressure from the upper airway musculature (Ayappa & Rapoport, 2002).

The influence of upper airway compliance on upper airway muscle characteristics can be accounted for by the influence of negative airway pressure on the activity of these muscles; the more compliant the upper airway tissues, the greater the decrease in the pharyngeal cross-sectional area with decreasing upper airway pressure, the greater the increase in airflow velocity with decreasing upper airway patency, with a further increase transmurul pressure gradient in a self-aggravating phenomenon. Therefore, the maintenance of upper airway patency during wakefulness requires a constant adaptation of upper airway dilator activity to counterbalance the destabilizing effect of the increase in upper airway collapsibility in Sleep apnea / hypopnoea syndrome (SAHS) (Series, 2002).

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20 2.9 Pathophysiology of the Upper Airway

Anatomic abnormalities of the pharynx are thought to play a role in the pathogenesis of obstructive sleep apnea. One key feature of sleep is suppression of upper airway muscle activity, and a sleep-related decrease in upper airway dilator muscle force is thought to lead pharyngeal narrowing or closure in patients with obstructive sleep apnea or hypopnea (Isono et al., 1997).

There is structural narrowing between either the area behind the soft palate and the posterior pharyngeal wall; including the uvula and the tonsils, or the area between the base of the tongue the posterior pharyngeal wall, or both sometimes, although not as frequently, the hypopharynx is also narrowed. What appears to happen is that the muscles, particularly the genioglossus, that keep the airway open in the waking state and are phasic inspiratory in nature become somewhat blunted in their response during sleep, allowing a narrowed airway to collapse. Then, the increased effort of the chest wall muscles builds up negative pressure in the lungs, and an arousal take place to break the cycle (Cartwright, 2001).

OSA occurs when the dilator muscles of the upper airway (geniohyiod, genioglossus, tensor veli palatine) lose their tone and are unable to offset the negative pressure of the inspiration which draws the base of tongue (including the epiglottis) and soft palate posteriorly against the pharyngeal walls (Friedlander et al., 2000). The inspiratory patency of the retropalatal, retroglossal, and retroepiglottic pharynx is caused by contraction of the

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tensor palatine, the genioglossus, and the hyoid bone muscles, respectively (Benumof, 2001).

The pharynx is patent at atmospheric intraluminal pressure in normal subjects, and requires negative intraluminal pressure for closure. In contrast, patients with obstructive sleep apnea had positive closing pressure, ie, the pharynx was closed at atmospheric intraluminal pressure. Hence, the surrounding extraluminal pressure is an important contributor to the collapsing transmurul pressure during sleep (Badr et al., 1999).

Upper-airway dysfunction and the specific sites of narrowing or closure are influenced by the underlying neuromuscular tone. Upper-airway size is determined by soft-tissue and skeletal factors that are also the major determinants of upper-airway patency during sleep.

In obese patients, increased adipose tissue in the neck may predispose the airway narrowing.

During sleep the neural impulses to pharyngeal dilator muscle are diminished, allowing the anatomical forces to increase pharyngeal collapsibility. Two hypotheses have been proposed to explain the maintenance of pharyngeal airway during sleep. The neural hypothesis proposes the loss of wakefulness stimulus and diminished neural drive to pharyngeal dilator muscles during sleep, promoting the highly compliant pharynx to narrow or collapse. The second hypothesis implicates the role of mechanical factors inherent in the pharynx as the mechanism of airway collapse (Mohesinin, 2003).

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The size of the pharyngeal lumen is determined by balance between outward forces developed by active contraction of upper airway muscles and inward forces resulting from subatmospheric luminal pressure during inspiration (Isono et al., 1997). The upper airway obstructions are classified for purpose of treatment: type I, an upper pharynx obstruction, involves the palate, uvula, and tonsils; type III, a lower pharynx obstruction, involves the tongue base and supraglottic structures; and type II is a combination of upper and lower obstructions (Waite, 1998).

2.9.1 Shape and Position of the Tongue

The tongue plays an important role in OSAS, in the supine position the tongue projects posteriorly by gravity, only counteracted by the tone of the genioglossal muscle (Figure 2.4). Herper (1976) and Sauerland (1978) have documented loss of tone in the genioglossal muscle during apnoeic periods and suggested that the posterior projection of the tongue onto the posterior pharyngeal wall accounts for the obstruction. Both the size and position of the tongue are important determinators wherther apnoeic periods are precipitated (Lyberg, 1989).

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The important role of the tongue in the pathogenesis of OSA has been confirmed in several studies. There is evidence that phasic respiratory activity of the phasic genioglossus is diminished in patients with OSA. This relaxation of the genioglossus during sleep would cause posterior displacement of the tongue, thus further occluding an already narrow airway it must be stressed that the genioglossus is only one of the muscles that are important in maintaining airway patency. Other muscle, such as the tensor palatine, which holds the soft palate up, and the masseter, which prevents the recession and rotation of the mandible during sleep, may also play an important role in the pathogenesis of OSA (Rivlin et al., 1983).

Figure 2.4 Abnormal airway during sleep (Adapted from American Academy of Family Physion, 1999)

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Electromyogram of the genioglossus during sleep has shown decreased activity in response to airway occlusion in nine premature infants with mixed obstructive and central apnea. A similar study in older children who had OSA secondary to tonsillar hypertrophy showed no decrease in genioglossus electromyogram activity at the onset of an obstructed breath however, there was an in increase in activity of the electromyogram at the end of the obstructive (Singer and Saenger, 1990).

Enlargement of the tongue as defined by the tongue extending about the level of the mandibular occlusal plane was associated with increased risk for OSA when controlled for other variables within the model but was not significant after controlling for body mass index and neck circumference ( Figure 2.5). Macroglossia is a common feature in individuals with Down syndrome and is likely to be a major factor in the increased prevalence of obstructive sleep apnea observed in this population.

There is a trend for patients with sleep disordered breathing to have larger tongue size compared with people without sleep disorder breathing, but tongue size is independent of AHI. Tongue size positively correlates with body mass index and neck circumference (Do et al., 2000).

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